Counter current mechanism and glomerulus - KIDNEY IN MD ANAESTHESIA RELAVENT

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counter current mechanism kidney loop of Henle diagram

This dual-panel fluorescence microscopy image (A and B) demonstrates the developmental orientation of the loop of Henle in cultured embryonic mouse kidney cortex (E11.5 + 7d). The visual captures two primary tubular systems: the branching collecting duct system, stained purple-blue (CalbindinD28k), and the developing loops of Henle, delineated by green and red signals. The green fluorescence (anti-laminin) marks the basement membranes of the tubules, while the red signal identifies Tamm-Horsfall Protein (THP), a marker for maturing loops of Henle. Solid white arrows highlight the hairpin-like terminal ends or 'tips' of these loops, where red THP expression is most intense. Dotted white arrows point to the primary branch points of the collecting duct network. The images illustrate a clear centripetal growth pattern, where the loops of Henle extend and orient themselves toward the oldest, largest junctions of the collecting duct system. This configuration serves as an educational model for renal morphogenesis and the spatial navigation of nephron segments during kidney development. Scale bars: 200 μm.

This digital schematic illustration depicts the molecular pathophysiology of autosomal recessive polycystic kidney disease (ARPKD). The image emphasizes a renal tubular epithelial cell with its primary cilium emanating from the apical membrane of a collecting duct/loop of Henle segment. The left side labels the PKHD1-encoded fibrocystin (fibrocystin/polyductin) protein localized to the ciliary membrane and apical plasma membrane, illustrating its role in the ciliopathy pathway alongside polycystin-1 (PC1) and polycystin-2 (PC2). The diagram highlights the basal body–transition zone complex, with DZIP1L positioned at centrioles and the distal basal body, underscoring its necessity for trafficking gene products into the ciliary axoneme. A transverse section inset shows microtubule axonemes and the ciliary pocket, connecting to the primary cilium’s sensory function. Arrows denote intracellular trafficking and-lumen orientation. Dysfunctions in fibrocystin and DZIP1L disrupt ciliary signaling, promoting cystogenesis in ARPKD and reflecting a ciliopathy mechanism shared with other cystic diseases. The illustration also notes that fibrocystin is variably expressed in pancreatic and bile duct epithelium, consistent with multisystem involvement. This visualization serves educational purposes for genetics, nephrology, and cell biology, and supports research into targeted therapies addressing ciliary assembly and trafficking defects. Clinicians and students can correlate genotype–phenotype concepts with this concise framework for learning.

This pathophysiology diagram illustrates the mechanism of IL-17A-mediated renal injury in diabetic nephropathy. The flowchart originates with 'Diabetes' leading to two concurrent pathways: the activation of immune cells and damage to resident renal cells (podocytes, mesangial cells, and endothelial cells). The immune pathway details the differentiation of CD4+ T-lymphocytes into Th17 cells, which infiltrate the kidney and produce local IL-17A. This cytokine acts back on injured renal cells, triggering a feedback loop that leads to the sustained production of inflammatory mediators and chronic renal inflammation. At the cellular level, the diagram highlights the effect of local IL-17A on tubular epithelial cells, depicting a morphological transition labeled as 'Partial EMT' (Epithelial-to-Mesenchymal Transition). Here, structured cuboidal tubular cells transform into elongated, spindle-shaped mesenchymal cells associated with extracellular matrix deposition, ultimately culminating in tubulointerstitial fibrosis. The visual summarizes the interplay between metabolic stress, Th17-driven inflammation, and structural remodeling in the progression of diabetic kidney disease.

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Kidney - Counter-Current Mechanism & Glomerulus (MD Anaesthesia)

Source: Morgan & Mikhail's Clinical Anesthesiology, 7e (the standard MD Anaesthesia text)

The Nephron - Overview

Each kidney contains ~1 million nephrons. A nephron has at least six specialised segments:

Renal corpuscle (glomerulus + Bowman's capsule)
Proximal convoluted tubule
Loop of Henle
Distal tubule
Collecting tubule
Juxtaglomerular apparatus

Nephrons are classified as cortical (shorter loops, ~80% of RBF) or juxtamedullary (long loops, deep into medulla, critical for concentration).

THE GLOMERULUS (Renal Corpuscle)

Structure

The renal corpuscle = glomerulus + Bowman's capsule.

Blood enters via single afferent arteriole and exits via single efferent arteriole
The glomerular capillary tuft provides a large surface area for filtration

Three-Layer Filtration Barrier

Layer	Detail
Endothelial cells	Fenestrated (70-100 nm pores); large - allow water, solutes, small proteins
Basement membrane (GBM)	Fused with epithelial basement membrane; negatively charged (favours cation filtration, repels albumin)
Epithelial cells (podocytes)	Interdigitate tightly - filtration slits ~25 nm; final barrier to large molecules

The net negative charge of the barrier favours filtration of cations over anions. This is why albumin (negatively charged) is normally excluded.

Mesangial Cells (Third Cell Type)

Contractile cells between the basement membrane and epithelial cells. They regulate glomerular blood flow:

Cause Contraction (Decrease GFR)	Cause Relaxation (Increase GFR)
Angiotensin II	ANP (atrial natriuretic peptide)
Vasopressin (ADH)	Prostaglandin E2
Norepinephrine	Dopaminergic agonists
Histamine, Endothelins
Thromboxane A2
Leukotrienes C4, D4

Anaesthesia relevance: Dopamine and fenoldopam (D1 agonists) dilate afferent AND efferent arterioles, increasing GFR - this is the basis for their renoprotective use.

Glomerular Filtration Pressure (Starling Forces)

Pressure	Value
Glomerular hydrostatic pressure	~60 mmHg (driving force)
Plasma oncotic pressure	~25 mmHg (opposing)
Renal interstitial pressure	~10 mmHg (opposing)
Net filtration pressure	~25 mmHg

GFP is ~60% of mean arterial pressure
~20% of plasma is filtered in each pass through the glomerulus (filtration fraction)
Afferent tone - inversely proportional to filtration pressure
Efferent tone - directly proportional to filtration pressure

GFR - Numbers to Know

Measurement	Normal Value
GFR (men)	120 ± 25 mL/min
GFR (women)	95 ± 20 mL/min
Renal plasma flow (RPF)	~660 mL/min
Renal blood flow (RBF)	~1200 mL/min (20-25% of cardiac output)
Filtration fraction (FF = GFR/RPF)	~20%

Measured by: Inulin clearance (gold standard - freely filtered, not secreted/reabsorbed). Creatinine clearance is the clinical approximation (slightly overestimates because tubules also secrete creatinine).

TUBULAR OVERVIEW (before Counter-Current)

Segment	% of Filtered Na+ Reabsorbed	Key Feature
Proximal tubule	65-75%	Isotonic reabsorption, Na-K-ATPase driven
Loop of Henle	15-20%	Counter-current multiplier
Distal tubule	~5%	Aldosterone, Ca2+/Mg2+ regulation
Collecting tubule	5-7%	ADH action, final urine concentration

THE COUNTER-CURRENT MECHANISM

This is the most important concept for urine concentration and a favourite exam topic.

Components of the System

Counter-current multiplier - Loop of Henle
Counter-current exchanger - Vasa recta (paired capillaries)

The Loop of Henle - Structural Basis

The loop has descending and ascending limbs. They run parallel and in opposite directions - this is the anatomical basis of the counter-current system.

Segment	Permeability	Function
Thin descending limb	Permeable to water, Na+, Cl-, urea	Water drawn out by hypertonic medullary interstitium → tubular fluid becomes progressively more concentrated as it descends
Thin ascending limb	Permeable to Na+, Cl-, urea; but NOT water	Passive Na+ leak into interstitium
Thick ascending limb	Impermeable to water and urea	Active Na+/K+/2Cl- reabsorption (NKCC2 cotransporter)

The thick ascending limb is the engine of the counter-current multiplier. It actively pumps out NaCl without water following - this creates the osmotic gradient.

The Counter-Current Multiplier - Step by Step

The diagrams below show how the system progressively builds up the medullary osmotic gradient:

Counter-current multiplier mechanism - osmolality values

Key points from this diagram:

At "time zero" (panel 1): all segments at 285 mOsm (isotonic)
The thick ascending limb generates a 200 mOsm gradient at any single level (its maximum pumping capacity)
As fluid flows, this single effect is multiplied by the counter-current flow arrangement
End result: the papilla reaches 1200 mOsm (vs. cortex at 285 mOsm)

The mechanism:

Thick ascending limb pumps NaCl out → medullary interstitium becomes hypertonic
Descending limb (permeable to water) - water moves out by osmosis → tubular fluid becomes concentrated (descending)
Concentrated fluid turns at the tip and enters the ascending limb
Ascending limb again pumps NaCl - further increasing medullary gradient
This is repeated continuously → progressive amplification (multiplication) of the gradient from cortex to papilla

The fluid leaving the loop of Henle (entering the distal tubule) is hypotonic (100-200 mOsm/L) - because the thick ascending limb removed solute without water.

Urea's Contribution

Urea also accumulates in the medullary interstitium (passively, via urea transporter in inner medullary collecting duct, stimulated by ADH) and contributes significantly (~50%) to the total 1200 mOsm papillary osmolality.

The Counter-Current Exchanger - Vasa Recta

The vasa recta are the capillaries that supply the renal medulla. They also run in a hairpin loop alongside the loop of Henle.

Without vasa recta: blood flowing straight through the medulla would wash away the osmotic gradient
With counter-current exchange: solutes diffuse into descending vasa recta and back out of ascending vasa recta - the gradient is preserved, not washed out
Low blood flow to the medulla is also essential for maintaining the gradient (high flow would dilute it)
The medulla consequently has a PO₂ of only ~15 mmHg - making it very vulnerable to ischaemia

ADH (Vasopressin) - The Master Switch

The collecting tubule normally has low water permeability. ADH (from posterior pituitary) inserts aquaporin-2 channels (AQP2) into the luminal membrane of collecting duct cells. This allows:

Water to flow down the osmotic gradient created by the counter-current multiplier
Tubular fluid equilibrates with the increasingly hypertonic medullary interstitium
Final urine concentration up to 1200 mOsm/L (maximally concentrated)

Without ADH (diabetes insipidus): water stays in the tubule → dilute urine (as low as 50-100 mOsm/L).

RENAL AUTOREGULATION & ANAESTHESIA IMPLICATIONS

Autoregulation

Maintained between MAP 80-180 mmHg via myogenic response of afferent arterioles
Tubuloglomerular feedback: macula densa senses NaCl delivery; ↑ NaCl → afferent constriction → ↓ GFR (negative feedback)
Prostaglandins (PGE2, PGD2, PGI2) are vasodilatory and protective - especially important during hypotension/ischaemia (NSAIDs abolish this protection)

Effects of Anaesthesia on Renal Function

Effect	Mechanism
↓ RBF, GFR, urine output	Both neuraxial and general anaesthesia (reversible if BP and volume maintained)
Fluid retention postoperatively	Endocrine response to surgery (↑ADH, ↑aldosterone, ↑renin-angiotensin)
Oliguria during laparoscopy	Pneumoperitoneum → ↑ IAP → renal vein/IVC compression + ↓CO + ↑renin/aldosterone/ADH
Sevoflurane (Compound A)	Nephrotoxic in animals at low fresh gas flow; use ≥2 L/min fresh gas flow as precaution
NSAIDs perioperatively	Block prostaglandin vasodilation → ↓ RBF under stress → AKI risk

Key Vasomotor Effects on the Kidney

Drug/Condition	Effect on Kidney
Dopamine, Fenoldopam	D1 receptor → dilate afferent + efferent arterioles; ↑ GFR and natriuresis
Angiotensin II	Constricts efferent > afferent; maintains GFR initially, but ↓ RBF
ACE inhibitors	Block Ang II → dilate efferent → ↓ GFR (hazardous in renal artery stenosis)
Norepinephrine	Afferent + efferent constriction → ↓ GFR
ANP	Dilates afferent, constricts efferent → ↑ GFR; also inhibits aldosterone

QUICK SUMMARY FOR EXAM

Glomerulus:

Three-layer filtration barrier (endothelium + GBM + podocytes)
Net negative charge → repels albumin
Filtration pressure = 60 mmHg; GFR ~120 mL/min
Mesangial cells regulate GFR; contract with AngII, dilate with ANP

Counter-current multiplier (Loop of Henle):

Thick ascending limb: active NaCl reabsorption, impermeable to water → builds medullary gradient
Descending limb: permeable to water → concentrates tubular fluid passively
End result: medullary papilla ~1200 mOsm; fluid leaving loop ~100-200 mOsm (hypotonic)

Counter-current exchanger (Vasa recta):

Hairpin capillaries trap solutes in medulla
Low medullary blood flow preserves gradient
PO₂ ~15 mmHg in medulla → ischaemia-prone

ADH closes the loop: makes collecting duct water-permeable → final urine concentration up to 1200 mOsm

Anaesthesia key points:

All anaesthetics transiently ↓ RBF/GFR - maintain BP and volume
NSAIDs are dangerous in hypovolaemic/hypotensive states
Dopamine/fenoldopam are D1 renal vasodilators
Laparoscopic pneumoperitoneum reliably causes oliguria (multifactorial)
Sevoflurane: use ≥2 L/min fresh gas flow

Morgan & Mikhail's Clinical Anesthesiology, 7e - Chapter 30 (The Renal System), pp. 1210-1231

Liver lobes- Anatomy, physiology, histological with portal circulation in md Anaesthesia

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Liver: Anatomy, Physiology, Histology & Portal Circulation - MD Anaesthesia

Primary Source: Morgan & Mikhail's Clinical Anesthesiology, 7e - Chapter 33: Hepatic Physiology & Anesthesia

PART 1: GROSS ANATOMY

Weight & Position

Largest organ in the body: ~1500 g in adults
Located in the right upper quadrant, fixed by hepatic veins and peritoneal ligaments
Covered by Glisson's capsule (fibrous connective tissue) under the visceral peritoneum

Ligaments (Peritoneal Reflections)

Ligament	Significance
Falciform ligament	Remnant of umbilical vein; runs from umbilicus to liver; divides left lobe; cephalad leaves cover suprahepatic IVC
Left triangular ligament	Fixes left lobe to diaphragm; divide to mobilise left lobe, exposing left IVC wall
Right triangular ligament	Fixes right lobe to right hemidiaphragm; divide to rotate liver left
Lesser omentum	Between stomach and liver; free right edge = hepatoduodenal ligament (portal triad)

Anatomical Lobes (Morphological)

The falciform ligament divides the liver into:

Right lobe (larger) - with two additional smaller lobes on its posterior-inferior surface:
- Caudate lobe (segment I) - lies between IVC and ligamentum venosum; has its own direct hepatic vein drainage to IVC
- Quadrate lobe (part of segment IV) - lies between gallbladder fossa and falciform ligament
Left lobe (smaller)

Surgical (Functional) Anatomy - Couinaud's Segments

Surgeons describe the liver based on blood supply, not surface anatomy.

The porta hepatis (point of bifurcation of hepatic artery and portal vein) defines the true surgical right and left lobes - Cantlie's line (a plane from gallbladder fossa to IVC).

The liver is divided into 8 independent functional segments (Couinaud), each with its own:

Inflow: portal vein branch + hepatic artery branch
Outflow: hepatic vein branch + bile duct

Couinaud segments I-VIII - Bailey & Love / Histology Atlas

Segments	Territory
I	Caudate lobe (independent drainage to IVC)
II, III	Left lateral section
IV (IVa, IVb)	Left medial section
V, VI	Right posterior inferior
VII, VIII	Right posterior/anterior superior

Surgical relevance: Couinaud's segmental anatomy allows anatomical resections of individual segments with minimal blood loss - critical knowledge for hepatic surgery anaesthesia.

PART 2: PORTAL CIRCULATION & HEPATIC BLOOD FLOW

Dual Blood Supply

The liver has a unique dual blood supply:

Hepatic blood flow showing portal vein, hepatic artery, hepatic veins, and IVC - Morgan & Mikhail

Vessel	% Blood Flow	% O₂ Delivery	Pressure	Character
Portal vein	70%	30-50%	7-10 mmHg	Nutrient-rich, partially deoxygenated
Hepatic artery	30%	50-70%	Systemic (~90 mmHg)	Oxygenated

Total hepatic blood flow = 25-30% of cardiac output (~1500 mL/min)

Formation of the Portal Vein

The portal vein forms behind the neck of the pancreas by the union of:

Superior mesenteric vein (from small bowel + right colon)
Splenic vein (from spleen; also receives inferior mesenteric vein)

It carries blood from:

Stomach, small intestine, large intestine (to splenic flexure)
Spleen, pancreas, gallbladder

Portal Vein at the Hilum

At the porta hepatis (hepatoduodenal ligament - free edge of lesser omentum), the structures in order (from front to back):

"BD-HA-PV" (Bile Duct - Hepatic Artery - Portal Vein)

Bile duct: anterior right
Hepatic artery: anterior left
Portal vein: posterior (largest, posteriormost)

Hepatic Artery Anatomy

Origin: Coeliac trunk → common hepatic artery → proper hepatic artery (after gastroduodenal artery branches off) → right and left hepatic arteries
Important variant: Right hepatic artery may arise from superior mesenteric artery (runs behind bile duct) - present in ~20% - critical to identify before clamping/ligating
Another variant: Left hepatic artery may arise from left gastric artery - present in ~10-15%

Reciprocal (Buffer) Response

A decrease in either hepatic arterial or portal venous flow triggers a compensatory increase in the other (hepatic arterial buffer response). This protects the liver against ischaemia but is limited.

Venous Drainage

Three hepatic veins (right, middle, left) drain into the IVC just below the diaphragm:

Right hepatic vein: drains segments V, VI, VII
Middle hepatic vein: drains segments IV, V, VIII
Left hepatic vein: drains segments II, III (and often IV)
Caudate lobe (segment I): direct small tributaries into IVC - independent of the three main veins

Anaesthesia relevance: Lowering CVP during liver resection (target CVP <5 mmHg) reduces hepatic venous pressure and hepatic blood volume, substantially reducing blood loss. Small changes in hepatic venous tone produce large shifts in blood volume (liver as a reservoir).

Liver as Blood Reservoir

Portal vein pressure is normally only 7-10 mmHg, but the low resistance of hepatic sinusoids allows high flow. The liver contains ~10-15% of total blood volume:

During haemorrhage: hepatic venous pressure falls → blood is mobilised from hepatic sinusoids into central circulation
In right heart failure: ↑ CVP → hepatic venous congestion → impaired liver function
During liver surgery: lowering CVP reduces hepatic blood volume and intraoperative bleeding

PART 3: HISTOLOGY

Overview of Liver Structure

The liver parenchyma is made up of 50,000-100,000 lobules.

The liver consists of four structural components:

Hepatocytes - arranged in anastomosing plates (one cell thick in adults)
Sinusoidal capillaries - between hepatocyte plates
Perisinusoidal spaces (Space of Disse) - between sinusoidal endothelium and hepatocytes
Connective tissue stroma - continuous with Glisson's capsule, carries portal tracts

Classic Hepatic Lobule

The traditional organisational unit - hexagonal prism of tissue:

Centre: Terminal hepatic venule (central vein)
Periphery (6 corners): Portal triads (portal canals)
Hepatocyte plates radiate from central vein to periphery, like spokes of a wheel
Sinusoids run between the plates, draining centripetally into the central vein
Size: ~2.0 mm × 0.7 mm

Portal Triad (Portal Canal)

Each corner of the hexagonal lobule contains a portal triad:

Structure	Contents
Portal venule	Branch of portal vein; carries nutrient-rich blood
Hepatic arteriole	Branch of hepatic artery; oxygenated blood
Bile ductule	Carries bile in opposite direction to blood flow
+ Lymphatics and nerves

The connective tissue of the portal canal is continuous with Glisson's capsule.

The Hepatic Lobule Diagram (Full Internal Structure)

Hepatic lobule - Morgan & Mikhail showing sinusoids, Kupffer cells, Space of Disse, bile canaliculi, central vein, portal triad

This diagram shows:

Portal triad (bile duct + hepatic artery branch + portal vein branch) at periphery
Sinusoids running radially toward the central vein
Space of Disse between sinusoids and hepatocytes
Kupffer cells lining the sinusoids
Bile canaliculi running between hepatocytes (opposite direction to blood flow)
Terminal lymphatics

Sinusoids

The sinusoids are capillaries between the hepatocyte plates
Blood from portal venules AND hepatic arterioles commingles in sinusoids before flowing to the central vein
Lined by fenestrated endothelial cells (large pores, no diaphragm - unlike other capillaries)
Kupffer cells (resident macrophages) are embedded in the sinusoidal lining - remove bacterial endotoxins, viruses, proteins, and particulate matter

Space of Disse

Perisinusoidal space between the endothelium and hepatocytes
Contains hepatic stellate cells (Ito cells) - store vitamin A; when activated, produce collagen (fibrosis/cirrhosis)
The space is in direct communication with lymphatic channels - a major site of lymph formation

Bile Canaliculi

Form between adjacent hepatocytes within each plate
Bile flows centrifugally (peripherally, toward bile ducts in portal triads) - opposite direction to blood
Bile canaliculi → bile ductules → interlobular bile ducts (in portal triads) → right/left hepatic ducts → common hepatic duct

Three Ways to Describe the Functional Unit

Unit	Centre	Periphery	Best for describing
Classic lobule	Central vein	Portal triads	Traditional description, histology
Portal lobule	Portal triad	Central veins	Exocrine (bile secretion) function
Liver acinus (Rappaport)	Terminal portal tract (short axis)	Two central veins	Blood flow, oxygenation, toxicology, pathology

The Liver Acinus - Most Clinically Relevant Unit

The acinus is the functional unit that best correlates with blood perfusion and liver pathology.

Hepatocytes are divided into three zones based on distance from the blood supply:

Zone	Location	Oxygenation	Clinical Significance
Zone 1 (periportal)	Closest to portal triad	Best oxygenated	First to show bile stasis changes; last to die with ischaemia; first to regenerate
Zone 2 (midzonal)	Intermediate	Intermediate	Intermediate features
Zone 3 (centrilobular/perivenous)	Closest to central vein	Least oxygenated	First to undergo ischaemic (centrilobular) necrosis; first to accumulate fat; most sensitive to volatile anaesthetic agents (zone 3 CYP2E1 activity)

Anaesthesia relevance (Zone 3): Halothane hepatotoxicity and drug-induced hepatocellular injury characteristically cause centrilobular necrosis (zone 3). Reduced hepatic blood flow during anaesthesia further compromises zone 3 hepatocytes.

PART 4: HEPATIC PHYSIOLOGY (MD Anaesthesia Focus)

Metabolic Functions

Function	Detail
Carbohydrate metabolism	Converts fructose/galactose to glucose; glycogen storage and release; gluconeogenesis
Protein synthesis	Albumin, clotting factors (all except VIII and vWF), alpha/beta globulins, transferrin, haptoglobin, ceruloplasmin
Fat metabolism	Fatty acid oxidation, cholesterol synthesis, bile acid synthesis, lipoproteins
Hormone metabolism	Converts T4 → T3 (active); degrades insulin, steroids (estrogen, aldosterone, cortisol), glucagon, ADH
Vitamin storage	A, B12, D, E, K
Drug metabolism	Phase I (CYP450) and Phase II (conjugation) reactions - critical for anaesthesia pharmacology
Detoxification	Kupffer cells remove endotoxins; urea synthesis from ammonia

Coagulation - Key Anaesthesia Knowledge

Liver synthesises all coagulation factors EXCEPT factor VIII and vWF (produced by endothelium/megakaryocytes)
Vitamin K-dependent factors: II, VII, IX, X, Protein C, Protein S (remember: "1972")
Factor VII has the shortest half-life (4-6 h) → PT prolonged first in acute liver failure
PT/INR measures synthetic function (fibrinogen, prothrombin, V, VII, X)
Important caveat: INR was designed for warfarin monitoring. In liver disease, anticoagulants (Protein C, S, Antithrombin III) are also reduced → the liver disease patient may be hypercoagulable or hypocoagulable - not simply one direction

Bilirubin Metabolism

Bilirubin (end-product of haem catabolism from Kupffer cells):

Unconjugated bilirubin released into blood → binds albumin
Passive hepatic uptake → intracellular binding traps it
Conjugated with glucuronide in hepatocytes
Actively excreted into bile canaliculi

Anaesthesia relevance: Postoperative jaundice is most commonly prehepatic (haematoma resorption, haemolysis post-transfusion). Halothane hepatotoxicity is the classic drug cause of hepatic jaundice.

Liver Function Tests - Interpretation for Anaesthesia

Test	Normal	Measures	Anaesthesia Relevance
ALT/AST (transaminases)	<40 IU/L	Hepatocellular necrosis/inflammation	High = hepatocellular damage, NOT synthetic function
Alkaline phosphatase	25-85 IU/L	Biliary obstruction; also bone	↑ in cholestasis
Serum albumin	3.5-5.5 g/dL	Chronic synthetic function (t½ = 2-3 weeks)	<2.5 g/dL = chronic liver disease/malnutrition
PT/INR	11-14 s / <1.2	Acute synthetic function (factor VII t½ = 4-6h)	>3-4 s above control = significant
Serum bilirubin	<17 μmol/L	Excretory function
Blood ammonia	47-65 mmol/L	Hepatic urea synthesis	↑ = severe hepatocellular damage/encephalopathy

PART 5: EFFECTS OF ANAESTHESIA ON HEPATIC FUNCTION

Effects on Hepatic Blood Flow

Agent/Condition	Effect	Mechanism
All general anaesthesia	↓ HBF up to 30-40%	↓ CO, ↓ portal flow, sympathetic activation
Surgery near liver	↓ HBF up to 60%	Sympathetic activation + direct vascular compression
Volatile agents (isoflurane)	Maintains HBF relatively well	Vasodilation of hepatic artery
Halothane	↓ HBF most of all volatiles	Portal flow reduction
High PEEP / positive pressure ventilation	↓ HBF	↓ CO, ↑ hepatic venous back pressure
Neuraxial (thoracic epidural)	Increases HBF after abdominal surgery	↓ sympathetic tone, improved splanchnic flow
Laparoscopy/pneumoperitoneum	↓ HBF	↑ IAP → portal vein compression
Sympathetic activation	↓ HBF	α1-adrenergic vasoconstriction of hepatic artery and mesenteric vessels
β-blockers	↓ HBF and portal pressure	Block β2 hepatic artery vasodilation
Vasopressin	↓ Splanchnic/portal blood flow	Splanchnic vasoconstriction (used in variceal bleeding)
Dopamine	↑ HBF (at low doses)	D1 receptor vasodilation

Halothane Hepatotoxicity

Two types:

Type I (mild): ~20% of patients; self-limiting transaminase rise; mechanism = reductive metabolism of halothane → free radical intermediates
Type II (fulminant): 1/10,000-1/35,000; immune-mediated; trifluoroacetyl hapten on hepatocyte proteins triggers immune response; centrilobular necrosis; higher risk with: multiple exposures, female sex, obesity, middle age, family history

Desflurane, sevoflurane, isoflurane: minimal to no direct hepatotoxic effect on hepatocytes.

Opioids and Sphincter of Oddi

All opioids can cause sphincter of Oddi spasm → ↑ biliary pressure → can mimic biliary colic or confuse intraoperative cholangiography
Treatment: naloxone or glucagon (relieves spasm)
Fentanyl causes less spasm than morphine; pethidine (meperidine) has the least effect

Neuroendocrine Stress Response

Surgery + anaesthesia → ↑ catecholamines, glucagon, cortisol → hyperglycaemia + catabolism (negative nitrogen balance)

Regional anaesthesia (neuraxial) has the most blunting effect on this response
Deep general anaesthesia and sympathetic blockade have a partial effect

Postoperative Jaundice - Classification

Type	Cause
Prehepatic (most common)	Haematoma resorption, transfusion haemolysis, senescent RBC breakdown
Hepatic	Pre-existing liver disease, ischaemia/hypoxaemia, halothane, drug reactions, Gilbert syndrome
Posthepatic	Bile duct injury, retained CBD stone, pancreatitis, cholecystitis

Portal Hypertension & Cirrhosis - Anaesthesia Implications

Portal hypertension (portal pressure >12 mmHg) → varices (oesophageal, gastric, rectal, umbilical) → haemorrhage risk.

Effects of cirrhosis relevant to anaesthesia:

System	Effect
Coagulation	↓ all clotting factors (except VIII), ↓ platelets (hypersplenism), ↑ PT/INR
Pharmacokinetics	↓ albumin → ↑ free drug fraction; ↓ CYP450 → ↓ drug metabolism; ↑ Vd (ascites)
Cardiovascular	Hyperdynamic circulation (high CO, low SVR); portopulmonary hypertension; hepatopulmonary syndrome
Renal	Hepatorenal syndrome; sodium and water retention
Respiratory	Pleural effusion (hepatic hydrothorax); restricted diaphragm (ascites)
Encephalopathy	↑ NH3; opioids/benzodiazepines worsen it
Drug metabolism	Avoid hepatically-metabolised drugs or reduce doses

QUICK EXAM SUMMARY

Gross anatomy:

4 morphological lobes (right, left, caudate, quadrate); 8 Couinaud surgical segments
Falciform ligament = anatomical left/right division; Cantlie's line = true surgical division
Caudate lobe has independent drainage direct to IVC

Portal circulation:

Portal vein = SMV + splenic vein; carries 70% of flow, 30-50% O₂
Hepatic artery = 30% flow, 50-70% O₂; comes from coeliac trunk
At porta hepatis: BD (right) - HA (left) - PV (posterior)
Hepatic arterial buffer response: compensatory ↑ when portal flow drops

Histology:

Classic lobule: hexagonal, central vein at centre, portal triads at corners
Blood flow: portal triad → sinusoids → central vein (centripetal)
Bile flow: canaliculi → ductules → ducts (centrifugal - opposite to blood)
Liver acinus zones: Zone 1 = periportal (survives ischaemia longest); Zone 3 = centrilobular (first to die from ischaemia; halothane hepatotoxicity here)

Anaesthesia key points:

All GA ↓ HBF 30-40%; surgery near liver ↓ HBF up to 60%
Low CVP strategy (< 5 mmHg) during hepatic resection reduces blood loss
Halothane = centrilobular necrosis; des/sevo/iso = minimal hepatotoxicity
All opioids → sphincter of Oddi spasm → treat with naloxone or glucagon
INR in liver disease ≠ bleeding tendency (anticoagulants also ↓)
Coagulation factors made by liver: ALL except factor VIII and vWF

Morgan & Mikhail's Clinical Anesthesiology, 7e - Chapter 33 (Hepatic Physiology & Anesthesia), pp. 1334-1360; Bailey & Love's Short Practice of Surgery, 28e - Chapter 69; Histology: A Text and Atlas, 8e - Chapter 18

Posterior triangle of neck , IJV , subclavian vein, femoral vein in MD ANESTHESIA

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internal jugular vein central line anatomy triangle sternocleidomastoid

This clinical photograph illustrates the surface anatomy of the neck and superior thoracic region, specifically highlighting the landmarks for central venous catheterization of the internal jugular vein. The image demonstrates Sedillot’s triangle, an anatomical space used for the central approach during puncture. Colored arrows delineate the triangle's boundaries: a yellow arrow indicates the medial border formed by the sternal head of the sternocleidomastoid muscle; an orange arrow indicates the lateral border formed by the clavicular head of the same muscle; and a red arrow marks the inferior border defined by the superior margin of the medial third of the clavicle. A black star designates the apex of this triangle, which serves as the primary anatomical site for cutaneous puncture. The image is an educational resource for medical students and clinicians to visualize critical surface landmarks required for safe vascular access, emphasizing the relationship between muscular structures and the clavicle in critical care and anesthesiology contexts.

This clinical photograph displays a close-up view of a patient's neck in the dorsal decubitus position, rotated contralaterally to expose the right cervical region. A blue ink marking delineates a triangle representing Sedillot's triangle, an anatomical landmark used for internal jugular vein (IJV) cannulation via the traditional technique (TT). The base of the triangle is situated inferiorly near the clavicle, while the two ascending sides correspond to the sternal and clavicular heads of the sternocleidomastoid muscle. The apex of the triangle is positioned superiorly where these two muscle heads converge. A specific circular mark near the apex indicates the intended puncture point for vascular access, which is clinically localized lateral to the palpated common carotid artery (CCA) pulse. The image serves as an educational guide for identifying superficial anatomical landmarks necessary for central venous catheterization and highlights the surface anatomy used in blind or ultrasound-guided vascular procedures within the field of anesthesiology and critical care.

A clinical photograph of the right lateral neck of a patient in a supine, head-down position, demonstrating surface anatomical landmarks for internal jugular vein (IJV) catheterization. Three 'X' markings are visible along a horizontal line at the level of the cricoid cartilage. The leftmost mark indicates the cricoid cartilage itself. The central mark, labeled 'M1' and indicated by a white arrow, represents the apex of the triangle formed by the sternal and clavicular heads of the sternocleidomastoid muscle. The lateral mark, labeled 'M2' and indicated by a black arrow, represents an alternative landmark identified by observing respiratory jugular venodilation and manual palpation of the IJV. The image illustrates the spatial relationship between traditional surface landmarks and dynamic physiological markers (venodilation) used to improve the accuracy of central venous access. Subtle skin elevations near M2 correspond to underlying venous distension, providing clinical guidance for needle insertion in the absence of ultrasound.

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Posterior Triangle of Neck, IJV, Subclavian Vein & Femoral Vein - MD Anaesthesia

Sources: Gray's Anatomy for Students 4e; Fischer's Mastery of Surgery 8e; Morgan & Mikhail's Clinical Anesthesiology 7e; Barash's Clinical Anesthesia 9e

PART 1: POSTERIOR TRIANGLE OF THE NECK

Boundaries

Posterior triangle of the neck - Gray's Anatomy for Students

The posterior triangle is on the lateral aspect of the neck, in continuity with the upper limb. It is divided by the inferior belly of omohyoid into two sub-triangles.

Boundary	Structure
Anterior	Posterior border of sternocleidomastoid (SCM)
Posterior	Anterior border of trapezius
Base (inferior)	Middle one-third of clavicle
Apex (superior)	Occipital bone, just posterior to mastoid process (where SCM and trapezius meet)
Roof	Investing layer of cervical fascia (between SCM and trapezius)

Sub-Triangles

The inferior belly of omohyoid (passing from scapula to hyoid, anchored by a fascial sling to the clavicle) subdivides the posterior triangle into:

Sub-Triangle	Location	Key Contents
Occipital triangle	Superior (larger)	Accessory nerve [XI], cervical plexus, brachial plexus
Omoclavicular (Subclavian) triangle	Inferior (smaller)	Subclavian artery (3rd part), subclavian vein, supraclavicular nerves

Muscular Floor

Covered by prevertebral fascia; from superior to inferior:

Splenius capitis
Levator scapulae
Posterior scalene
Middle scalene (most important - subclavian artery passes between anterior and middle scalene)
Anterior scalene

Contents - Vessels

Vessel	Detail
External jugular vein	Most superficial; crosses SCM → enters posterior triangle → pierces investing fascia → drains into subclavian vein
Subclavian artery (3rd part)	Crosses the base; emerges lateral to anterior scalene → becomes axillary artery at lateral border of rib I
Transverse cervical artery	Branch of thyrocervical trunk; crosses base anteriorly
Suprascapular artery	Branch of thyrocervical trunk; crosses base
Subclavian vein	Just below/at base; anterior to anterior scalene (anterior to the artery!)

Contents - Nerves

Accessory nerve and cervical plexus branches in posterior triangle

Nerve	Path	Clinical Significance
Accessory nerve [XI]	Exits jugular foramen → passes through/behind SCM → crosses posterior triangle obliquely → enters trapezius	Very superficial - at risk during neck dissection and CVC placement
Cervical plexus (C1-C4)	Cutaneous branches emerge at posterior border of SCM	Lesser occipital, great auricular, transverse cervical, supraclavicular nerves
Phrenic nerve (C3,4,5)	Crosses anterior scalene from lateral to medial → descends into thorax	Risk with supraclavicular brachial plexus block; interscalene block
Brachial plexus (C5-T1)	Roots exit between anterior and middle scalene muscles; trunks cross the posterior triangle	Target for interscalene / supraclavicular nerve blocks

Anaesthesia relevance: The posterior triangle is the approach zone for:

Interscalene brachial plexus block

Supraclavicular brachial plexus block

External jugular vein cannulation

Subclavian vein (supraclavicular approach)

Risk of pneumothorax and phrenic nerve palsy with blocks in this region

PART 2: INTERNAL JUGULAR VEIN (IJV)

Anatomy

Origin: At the jugular foramen in the base of the skull (continuation of sigmoid sinus)
Course: Descends within the carotid sheath alongside the common carotid artery and vagus nerve
Relationship: Lies lateral to the common carotid artery (CCA) and internal carotid artery (ICA) in the upper neck; becomes anterolateral to CCA in the lower neck
Termination: Joins the subclavian vein behind the medial end of the clavicle (medial to anterior scalene) → forms the brachiocephalic (innominate) vein

The Sedillot Triangle (IJV Cannulation Landmark)

The central approach uses the triangle formed by the two heads of SCM:

Sedillot's triangle - surface anatomy for IJV cannulation

Border	Structure
Medial border	Sternal head of SCM (yellow arrow)
Lateral border	Clavicular head of SCM (orange arrow)
Base (inferior)	Superior margin of medial third of clavicle (red arrow)
Apex (★)	Convergence of two heads - needle insertion point

The IJV at this point lies just lateral to the carotid pulse - the carotid pulsation is used to identify and displace the artery medially.

Approaches to IJV Cannulation

Approach	Needle Entry Point	Direction	Preferred
Central (most common)	Apex of Sedillot's triangle (between two heads of SCM, at level of thyroid cartilage)	30-45° toward ipsilateral nipple	Yes - most used
Anterior	Anterior border of SCM, at the level of thyroid cartilage	Toward ipsilateral nipple at 30-45°	Used
Posterior	Posterior border of SCM at junction of upper and middle thirds	Toward suprasternal notch	Less common

Patient Positioning for IJV

Trendelenburg (15-20°): Distends the vein, reduces air embolism risk
Head turned 30-45° to opposite side: Straightens the vessel, displaces it from behind SCM
Avoid excessive rotation (>45°) - compresses the vein

Advantages of IJV (for MD Anaesthesia Exams)

Advantage	Detail
Lower pneumothorax risk (~0.5%) vs. subclavian (~1.5%)	Lung apex not in the needle path
Compressible if arterial puncture occurs	External pressure can be applied
Right IJV preferred	Straight, direct route to SVC → right atrium; no angulation
Good for Swan-Ganz catheter	Direct path to right heart
Suitable for temporary pacemaker wires	Same reason

Disadvantages of IJV

Difficult in short/obese necks
Carotid artery puncture risk
Uncomfortable for patients (neck area)
Infection/thrombosis risk higher than subclavian for long-term use
Left IJV: risk of thoracic duct injury (chylothorax)

Depth to SVC-RA Junction (Formula - Fischer's)

Side	Vessel	Formula
Right	IJV	H/10 (cm), where H = height in cm
Right	Subclavian	H/10 - 2
Left	IJV	H/10 + 4
Left	Subclavian	H/10 + 2

Structures at Risk with IJV Cannulation

Structure	Complication
Common carotid artery	Arterial puncture, haematoma, pseudoaneurysm
Vagus nerve	Nerve injury (rare)
Sympathetic chain	Horner's syndrome (rare)
Thoracic duct (left)	Chylothorax
Lung apex	Pneumothorax (less common than subclavian)
Accessory nerve	Nerve injury (posterior approach)

PART 3: SUBCLAVIAN VEIN

Anatomy

Continuation of axillary vein from the lateral border of rib I
Crosses the anterior surface of the anterior scalene muscle (the artery passes posterior to it - this is the key anatomical fact: vein is anterior to the anterior scalene, artery is posterior to it)
Passes over rib I in the omoclavicular triangle, anterior to the anterior scalene muscle
Joins IJV behind the medial end of the clavicle to form the brachiocephalic vein
The vein is held patent by its attachment to the deep surface of the clavicle and the investing fascia - it does not collapse, making it accessible

Relationships at Site of Cannulation

Structure	Position Relative to Subclavian Vein
Clavicle	Superiorly (the vein passes behind/below the clavicle)
Rib I	Inferiorly
Anterior scalene	Posterior (the artery runs behind it; vein runs in front)
Subclavian artery	Posterior (separated by anterior scalene)
Phrenic nerve	Just posterior (on anterior scalene surface)
Brachial plexus	Posterior and lateral
Pleura	Inferoposterior - risk of pneumothorax

Infraclavicular Approach (Classic)

Patient position: Slight Trendelenburg + shoulder roll (pushes clavicle posteriorly)
Needle insertion: 1 cm below junction of medial and middle thirds of clavicle
Direction: Walk under the clavicle, aim toward the suprasternal notch
Bevel should face caudally to direct catheter away from the IJV toward the SVC
Advance until blood flashback, then rotate bevel 90° for passage

Supraclavicular Approach (less common)

Needle insertion: 1 cm lateral to SCM and 1 cm above the clavicle, in the omoclavicular triangle
Aimed at the junction of subclavian vein and IJV
Shorter path; some advantages in mechanically ventilated patients

Advantages of Subclavian Vein

Advantage	Detail
Most comfortable for long-term access	Away from neck movements
Lowest infection rate of all CVC sites	Least CLABSI risk; preferred for long-term catheters, PICC, implanted ports
Consistent anatomy	Vein does not collapse
Suitable when neck immobilised	Trauma, C-spine injury
Good for long-term parenteral nutrition

Disadvantages of Subclavian Vein

Disadvantage	Detail
Highest pneumothorax risk	1.5% (vs IJV 0.5%)
Non-compressible if arterial puncture	Clavicle prevents direct pressure → haematoma
Haemothorax risk
Risk of pinch-off syndrome	Catheter compressed between clavicle and rib I
Lower success rate in obese/short neck
Absolute contraindication: unilateral lung pathology	Contralateral pneumothorax would be fatal

PART 4: FEMORAL VEIN

Anatomy

The femoral vein lies within the femoral sheath (a funnel-shaped fascial prolongation of the transversalis fascia) below the inguinal ligament.

Femoral Sheath Contents (Lateral to Medial)

The mnemonic "NAVY" (from lateral to medial):

Compartment	Contents
N - Nerve	Femoral nerve (outside the sheath, lateral compartment)
A - Artery	Femoral artery (intermediate compartment)
V - Vein	Femoral vein (medial compartment)
Y - lymphatics (empty space)	Femoral canal (most medial - potential for femoral hernia)

The femoral vein is medial to the femoral artery and lateral to the femoral canal.

Surface Anatomy for Femoral Vein Cannulation

ASIS to pubic tubercle = inguinal ligament
Midpoint of inguinal ligament = femoral artery pulse
Femoral vein = 1-2 cm medial to femoral artery pulse, below inguinal ligament
Insert needle 1-2 fingerbreadths below the inguinal ligament, medial to the femoral arterial pulse
Direction: 30-45° angle, aimed cranially

Advantages of Femoral Vein

Advantage	Detail
Easiest and fastest access	Vein large; artery always palpable as landmark
No pneumothorax / no haemothorax risk	Away from chest
Preferred in emergency (cardiac arrest, trauma)	No need to interrupt CPR
Safe with coagulopathy (compressible)	Direct pressure can be applied
Alternative when neck/chest access impossible	Trauma, burns, previous bilateral CVC failure

Disadvantages of Femoral Vein

Disadvantage	Detail
Highest infection rate (CLABSI)	Groin colonisation with gut flora; avoid if possible in ICU
Highest DVT rate	Up to 15% symptomatic DVT; embolic risk
CVP measurement inaccurate	Too far from right atrium
Mixed venous O₂ (SvO₂) unreliable	Reflects lower body, not global; cannot use for DO₂ assessment
Limited mobility / patient discomfort
Contraindicated if abdominal/pelvic pathology	IVC thrombosis, trauma to iliac vein

PART 5: COMPARATIVE TABLE (MD ANAESTHESIA EXAM FAVOURITE)

Feature	IJV	Subclavian	Femoral
Preferred approach	Right central	Infraclavicular	Below inguinal ligament
Pneumothorax	0.5%	1.5% (highest)	None
Infection risk	Intermediate	Lowest (long-term)	Highest
DVT risk	Low	Low	Highest
Arterial puncture	Carotid (compressible)	Subclavian (non-compressible!)	Femoral (compressible)
CVP accuracy	Excellent	Excellent	Poor (too distal)
SvO₂ reliability	Good	Good	Poor
Emergency access	Good	Difficult in arrest	Best (CPR uninterrupted)
Coagulopathy	Caution	Avoid	Preferred
Long-term/TPN	Acceptable	Preferred	Avoid
Ultrasound guidance	Strongly recommended	Recommended	Recommended
Thoracic duct (left)	At risk	At risk	Safe

PART 6: SELDINGER TECHNIQUE (Common to All Sites)

Position patient appropriately (Trendelenburg for IJV/subclavian)
Prep and drape; ultrasound to identify vessel in-plane
Infiltrate local anaesthetic
Insert finder needle (22G) - confirm venous blood (non-pulsatile, dark)
Insert introducer needle (18G) - confirm venous blood
Pass J-tipped guidewire through needle (no resistance should be felt); confirm on ECG if available (P-wave morphology changes if wire in RA)
Remove needle over guidewire (never let go of guidewire!)
Dilate tract with dilator
Thread catheter over guidewire to appropriate depth
Remove guidewire; flush and aspirate all lumens
Secure catheter; apply dressing
Confirm position with chest X-ray (tip at cavo-atrial junction, no pneumothorax)

PART 7: COMPLICATIONS OF CENTRAL VENOUS CATHETERS

Immediate / Technical

Complication	Risk Factors	Comment
Pneumothorax	Subclavian > IJV	Commonest technical complication; risk ↑ 6x with ≥3 attempts
Arterial puncture	All sites	If dilator/catheter inserted into artery - DO NOT REMOVE, seek surgical help
Haematoma	Coagulopathy, multiple attempts	IJV/femoral compressible; subclavian non-compressible
Air embolism	Any site	Trendelenburg position prevents it; treat with Durant manoeuvre + aspiration
Haemothorax	Subclavian
Guidewire loss	Careless technique	Never let go of the guidewire
Cardiac arrhythmias	Guidewire too far	Wire irritates right ventricle → VT; watch ECG during insertion
Thoracic duct injury	Left IJV, left subclavian	Chylothorax

Air Embolism Management (Classic Exam Question)

Clamp catheter immediately
Left lateral decubitus + Trendelenburg (Durant's manoeuvre) - traps air in right ventricle away from pulmonary outflow
Aspirate air through catheter
100% O₂
Cardiopulmonary resuscitation if cardiovascular collapse
Hyperbaric oxygen if available

Late Complications

Complication	Detail
CLABSI	≥48h in situ; organisms migrate from skin or hub contamination
Catheter thrombosis	Up to 15%; treat with anticoagulation
Catheter malposition	Tip in azygous, internal mammary, contralateral brachiocephalic; verify on CXR
Pinch-off syndrome	Subclavian only; catheter compressed between clavicle and rib I
Catheter fracture / embolism	Remove under fluoroscopy

CLABSI Prevention Bundle (CDC/AHRQ)

Hand hygiene
Maximal sterile barrier (full gown, gloves, mask, cap, large drape)
Chlorhexidine skin prep (>0.5% in >70% alcohol)
Optimal site selection (avoid femoral when possible)
Daily review of necessity + remove when no longer required

QUICK EXAM SUMMARY

Posterior triangle:

Borders: SCM (anterior), Trapezius (posterior), Clavicle (base)
Subdivided by omohyoid → occipital (large, superior) + omoclavicular/subclavian triangle (small, inferior)
Key nerves: Accessory [XI] (most vulnerable), cervical plexus, phrenic nerve on anterior scalene, brachial plexus between scalenes
Key vessel: Subclavian artery (3rd part) at base; subclavian vein anterior to anterior scalene

IJV:

Sedillot's triangle (central approach); apex = needle entry point, lateral to carotid pulse
Right side preferred (straight path to SVC)
Lowest pneumothorax of the three sites
Depth formula: H/10 cm (right IJV); H/10+4 (left IJV)

Subclavian:

Vein is anterior to anterior scalene; artery is posterior to it
Highest pneumothorax risk (1.5%); non-compressible artery = dangerous if arterial puncture
Lowest long-term infection rate → preferred for TPN, long-term CVC
Formula: H/10-2 (right); H/10+2 (left)

Femoral:

NAVY: Nerve-Artery-Vein-lymphatics (lateral to medial)
Best for emergency/coagulopathy; NO pneumothorax
Highest infection and DVT rate; CVP and SvO₂ unreliable
Never first choice in ICU

Air embolism: Durant's manoeuvre = left lateral decubitus + Trendelenburg

Gray's Anatomy for Students, 4e - pp. 1163-1169; Fischer's Mastery of Surgery, 8e - pp. 319-330; Morgan & Mikhail's Clinical Anesthesiology, 7e - Chapter 5; Barash's Clinical Anesthesia, 9e - Chapter 26

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